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Department of Neuropharmacology, Glaxo Group Research Ltd, Ware, Hertfordshire.

1. The effects of prostaglandin E2 (PGE2) on ion transport were investigated in guinea-pig isolated gastric mucosa. 2. Under resting conditions the mucosa produced a short-circuit current (SCC), the majority of which could be attributed to electrogenic chloride secretion. This interpretation was confirmed by the dependence of the basal SCC on extracellular chloride, and inhibition by the chloride channel blocker, diphenylamine-2-carboxylate. The mucosa also exhibited low rates of acid secretion and of sodium and rubidium absorption. 3. PGE2 stimulated an increase in net chloride secretion which was more than sufficient to account for the concomitant increase in SCC. As with the basal SCC, the SCC response to PGE2 was chloride dependent and inhibited by diphenylamine-2-carboxylate. PGE2 also significantly increased acid secretion and net rubidium absorption, but these changes were not sufficient to account for SCC. 4. The H+-K+-ATPase inhibitor, omeprazole, inhibited basal and PGE2-stimulated acid secretion, but did not modify the effects the PGE2 on net chloride secretion, SCC or conductance, suggesting that these effects of PGE2 were not related to changes in gastric acid secretion. 5. Both basal and PGE2-stimulated SCC were dependent on extracellular sodium and inhibited by ouabain, indicating the importance of a sodium gradient and the Na+-K+-ATPase in maintaining the electrogenic properties of the mucosa. 6. These results are consistent with the view that PGE2 stimulates electrogenic chloride secretion in guinea-pig gastric mucosa, and provide an ionic basis for the stimulation of secretion of sodium and chloride by prostaglandins observed in mammalian gastric mucosa in vivo.